Field of the Invention
This invention relates to immune modulation oriented therapies for treating autoimmune disorders, and more specifically, to combination treatment therapies for ameliorating autoimmune toxicity in immune-mediated diseases.
Background Information
The following description includes information that may be useful in understanding the present invention. It is not an admission that any such information is prior art, or relevant, to the presently claimed inventions, or that any publication specifically or implicitly referenced is prior art.
Recent therapies for treating rheumatoid arthritis and other human autoimmune diseases have been based on non-specific suppression of the immune system. Treatment regimens so based target inflammatory immune pathways which result in having to be concerned with balancing toxicity caused by the non-specificity with the intended perceived benefits of disease remission.
For example, with respect to rheumatoid arthritis, first generation biologic agents have included those that interfere with the inflammatory cascade by blocking one or another component, for example an inflammatory cytokine such as TNFα. Such direct biological interference with pathogenic pathways is being considered for an ever-increasing number of molecules, primarily cytokines, to replace generalized pharmacological immunosuppression for a more tailored treatment route.
Given the further understanding that recognition of self is a physiologic and necessary phenomenon, and that “quality” and “intensity” of the immune responses is regulated by complex mechanisms that ensure that recognition of self does not lead to damage, and that necessary inflammatory responses, aimed at clearing perceived “danger” such as an infection, are down regulated once “danger” is eliminated, there is a need in the art for treatment regimens which take into account the complex set of complementary and interactive pathways that contribute to the qualitative and quantitative regulation of immune responses in order to prevent tissue damage. In this context affecting the immune system towards tolerance is akin to employing a dimmer switch; i.e., rather that causing complete on/off shifting of pathways, the reactivity is lessened. Thus, further treatment regimens focused on tolerance pathways should consider this complexity in order not to bring about toxic immune reactivity.
Some tolerance pathway-focused treatment regimens, such as in therapies for rheumatoid arthritis, are not antigen specific. Data suggests that blunting, or dimming down immune responses in a non-specific fashion may lead to undesirable effects with regard to frequency and gravity of occurrence which obviously varies according to the individual therapy and regimen. Thus, a need still exists in the art for a treatment method and therapeutic formulations and compositions to advance the immune treatment arts.